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Aims/hypothesis No established blood-based biomarker exists to monitor diabetic sensorimotor polyneuropathy (DSPN) and evaluate treatment response. The neurofilament light chain (NFL), a blood biomarker of neuroaxonal damage in several neurodegenerative diseases, represents a potential biomarker for DSPN. We hypothesised that higher serum NFL levels are associated with prevalent DSPN and nerve dysfunction in individuals recently diagnosed with diabetes. Methods This cross-sectional study included 423 adults with type 1 and type 2 diabetes and known diabetes duration of less than 1 year from the prospective observational German Diabetes Study cohort. NFL was measured in serum samples of fasting participants in a multiplex approach using proximity extension assay technology. DSPN was assessed by neurological examination, nerve conduction studies and quantitative sensory testing. Associations of serum NFL with DSPN (defined according to the Toronto Consensus criteria) were estimated using Poisson regression, while multivariable linear and quantile regression models were used to assess associations with nerve function measures. In exploratory analyses, other biomarkers in the multiplex panel were also analysed similarly to NFL. Results DSPN was found in 16% of the study sample. Serum NFL levels increased with age. After adjustment for age, sex, waist circumference, height, HbA 1c , known diabetes duration, diabetes type, cholesterol, eGFR, hypertension, CVD, use of lipid-lowering drugs and use of non-steroidal anti-inflammatory drugs, higher serum NFL levels were associated with DSPN (RR [95% CI] per 1-normalised protein expression increase, 1.92 [1.50, 2.45], p <0.0001), slower motor (all p <0.0001) and sensory (all p ≤0.03) nerve conduction velocities, lower sural sensory nerve action potential ( p =0.0004) and higher thermal detection threshold to warm stimuli ( p =0.023 and p =0.004 for hand and foot, respectively). There was no evidence for associations between other neurological biomarkers and DSPN or nerve function measures. Conclusions/interpretation Our findings in individuals recently diagnosed with diabetes provide new evidence associating higher serum NFL levels with DSPN and peripheral nerve dysfunction. The present study advocates NFL as a potential biomarker for DSPN. Graphical abstract

Background and purpose Various electrodiagnostic criteria have been developed in Guillain–Barré syndrome (GBS). Their performance in a broad representation of GBS patients has not been evaluated. Motor conduction data from the International GBS Outcome Study (IGOS) cohort were used to compare two widely used criterion sets and relate these to diagnostic amyotrophic lateral sclerosis criteria. Methods From the first 1500 patients in IGOS, nerve conduction studies from 1137 (75.8%) were available for the current study. These patients were classified according to nerve conduction studies criteria proposed by Hadden and Rajabally. Results Of the 1137 studies, 68.3% (N = 777) were classified identically according to criteria by Hadden and Rajabally: 111 (9.8%) axonal, 366 (32.2%) demyelinating, 195 (17.2%) equivocal, 35 (3.1%) inexcitable and 70 (6.2%) normal. Thus, 360 studies (31.7%) were classified differently. The areas of differences were as follows: 155 studies (13.6%) classified as demyelinating by Hadden and axonal by Rajabally; 122 studies (10.7%) classified as demyelinating by Hadden and equivocal by Rajabally; and 75 studies (6.6%) classified as equivocal by Hadden and axonal by Rajabally. Due to more strictly defined cutoffs fewer patients fulfilled demyelinating criteria by Rajabally than by Hadden, making more patients eligible for axonal or equivocal classification by Rajabally. In 234 (68.6%) axonal studies by Rajabally the revised El Escorial (amyotrophic lateral sclerosis) criteria were fulfilled; in axonal cases by Hadden this was 1.8%. Conclusions and discussion This study shows that electrodiagnosis in GBS is dependent on the criterion set utilized, both of which are based on expert opinion. Reappraisal of electrodiagnostic subtyping in GBS is warranted.

This study investigates the impact of the anatomical separation point of the dorsal ulnar cutaneous nerve (DUCN) on nerve conduction studies (NCS). Involving 25 subjects with DUCN NCS findings, it utilizes ultrasound to mark the DUCN's divergence from the ulnar nerve. NCS was performed at four points relative to the separation point. The findings indicate the maximal amplitudes occurred 2 cm distal to the separation point. The study suggests it is ideal when the stimulation is performed between the seperation point and 2 cm distal to it.

Xiaojuan Li,1,* Xing Zhao,2,* Yongpan Huang,3 Jiayu Tang1 1Department of Neurology, Brain Hospital of Hunan Province (The Second People’s Hospital of Hunan Province), Changsha, Hunan, 410007, People’s Republic of China; 2Department of Rehabilitation, Changsha Central Hospital, Changsha, Hunan, People’s Republic of China; 3Medicine School, Changsha Social Work College, Changsha, Hunan, 410004, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yongpan Huang, Medicine School, Changsha Social Work College, Changsha, Hunan, 410004, People’s Republic of China, Email yongpanhuangyxy@163.comBackground: Alzheimer’s disease (AD) and late-life depression (LLD) patients both exhibit peripheral motor nerve conduction impairments, but with distinct patterns, highlighting divergent neurophysiological mechanisms in these aging-related disorders.Objective: To compare peripheral nerve conduction function among normal cognition (NC), older adults with AD, and LLD.Methods: All the participants were enrolled and assigned to AD, LLD and aged-matched NC controls (all ≥ 60 years, n=60, respectively). Sensory conduction of the median and sural nerves, and motor conduction of the median and common peroneal nerves, were assessed. Key parameters included latency, amplitude, and conduction velocity. Group differences were analyzed after adjusting for gender, age, education, height, and comorbid medical conditions.Results: By controlling gender, age, height, education level, and somatic diseases with inter-group differences, compared with NC group, the median nerve motor conduction in AD group showed prolonged proximal latency (3.21 vs. 3.65 ms, P=0.023), reduced amplitude (proximal: 7.30± 2.02 vs. 3.89± 0.57 mV; distal: 6.13± 2.17 vs. 4.12± 2.38 mV, both P< 0.001), and slowed conduction velocity (56.46± 5.18 vs. 49.29± 6.27 m/s, P=0.002). LLD group exhibited more pronounced latency prolongation (proximal: 3.21 vs. 4.06 ms; distal: 7.18 vs. 7.98 ms, both P< 0.001) and greater amplitude reduction (proximal: 7.30± 2.02 vs. 3.65± 0.66 mV; distal: 6.13± 2.17 vs. 3.18± 1.88 mV, both P< 0.001). In terms of the common peroneal nerve motor conduction, function AD group had significantly slower conduction velocity (48.88± 5.82 vs. 42.85± 5.27 m/s, P=0.033). LLD group showed prolonged proximal latency (4.25 vs. 5.77 ms, P< 0.001). No significant differences were found in sensory conduction parameters across groups after adjustment.Conclusion: Both AD and LLD groups were associated with peripheral motor neuropathy, but the pattern of impairment differs. AD is marked by generalized conduction slowing, while LLD shows more severe latency delays and amplitude loss, suggesting distinct pathophysiological pathways. These findings provide new insights into the peripheral nervous system’s involvement in age-related neurocognitive and mood disorders.Keywords: nerve motor conduction, nerve sensory conduction, nerve conduction velocity, late-life depressive disorder, Alzheimer’s disease

We examined the causes of decreased fingertip dexterity in elderly individuals with an aim to improve their quality of life by improving their activities of daily living. We calculated nerve conduction velocity, absolute error during force adjustment tasks, and fingertip dexterity test scores for 30 young (21–34 years old) and 30 elderly (60–74 years old) participants to identify age-related changes. We also assessed subjective complaints of pain, motor function, and numbness. Motor nerve (young: 55.8 ± 3.7 m/s; elderly: 52.2 ± 5.0 m/s) and sensory nerve (young: 59.4 ± 3.4 m/s; elderly: 55.5 ± 5.3 m/s) conduction velocities decreased in an age-dependent manner. Moreover, the decrease of motor nerve conduction velocity was associated with decreased fingertip dexterity (objective index), while the decrease of sensory nerve conduction velocity was associated with subjective complaints of pain and motor function (subjective index).

Diabetic peripheral neuropathy (DPN) is a common complication of type 2 diabetes mellitus (T2DM) and is closely linked to immune and inflammatory dysregulation. Multi-component pharmacological interventions have been explored as complementary approaches for metabolic and immune modulation; however, their effects on DPN and related mechanisms remain incompletely understood. A rat model of T2DM-associated peripheral neuropathy was established, and a multi-component pharmacological intervention (MPCI) was administered for 8 weeks. Peripheral nerve dysfunction was evaluated by motor and sensory nerve conduction velocities (MNCV and SNCV), behavioral outcomes, and histological/ultrastructural assessments. In parallel, spleen tissues were collected for transcriptomic profiling. RNA sequencing was performed to identify differentially expressed genes and immune-related pathways, and representative molecules involved in inflammatory regulation were further validated using western blotting and quantitative real-time PCR in sciatic nerve tissue. MPCI administration significantly ameliorated peripheral nerve dysfunction in T2DM rats, as evidenced by improved nerve conduction velocities and pathological features. Transcriptomic analysis of spleen tissue revealed that MPCI was associated with broad remodeling of diabetes-related immune and inflammatory gene programs. In parallel, sciatic nerve analyses showed attenuation of NF-κB/c-Jun-associated inflammatory signaling and modulation of inhibitory regulators at both the protein and mRNA levels. These findings indicate that MPCI improves T2DM-associated DPN and is associated with splenic immune remodeling and attenuation of peripheral nerve inflammatory signaling, providing exploratory evidence for associations between splenic immune transcriptomic remodeling and peripheral nerve inflammatory signaling.

Background Objective biochemical markers for stratifying brachial plexus injury (BPI) severity remain lacking. Platelet-activating factor (PAF), an inflammatory mediator implicated in neurological damage, has not been evaluated in traumatic BPI. We investigated whether serum PAF levels predict complete injury and correlate with nerve conduction impairment. Methods This retrospective case-control study analyzed 102 traumatic BPI patients (43 complete, 59 incomplete) and 51 matched controls enrolled between January 2020 and December 2023. Serum PAF and nerve conduction velocities (NCV) of median, radial, and ulnar nerves were measured. Multivariable logistic regression, restricted cubic spline (RCS) modeling, and ROC analysis were performed. Results BPI patients exhibited elevated PAF versus controls (171.8±26.1 vs. 147.7±12.1 pg/mL, P <0.001) and reduced mean NCV (19.8±2.6 vs. 64.0±6.1 m/s, P <0.001).PAF correlated inversely with NCV (ρ=-0.50, P <0.001). Complete injuries showed higher PAF (189.3±23.5 vs. 158.9±19.8 pg/mL, P<0.001) and lower NCV (all P<0.001). PAF (OR=1.151 per pg/mL, 95% CI: 1.033–1.284, P=0.011) and mean NCV (OR=0.012, P=0.014) independently predicted complete injury. RCS analysis revealed a nonlinear threshold at 165 pg/mL (OR=5.247, 95% CI: 2.808-9.803). PAF achieved good discrimination (AUC=0.840, sensitivity 84%, specificity 68%), though inferior to NCV (AUC=0.982). A multivariable model combining PAF, NCV, and injury-to-detection interval reached near-perfect discrimination (AUC=0.997). Conclusions Serum PAF independently predicts complete BPI with a nonlinear threshold at 165 pg/mL. While electrophysiological assessment remains the gold standard, PAF demonstrates potential as a rapid, minimally invasive screening tool in acute settings where immediate nerve conduction studies are unavailable, particularly for triaging patients requiring urgent intervention.

The median and ulnar nerves have been suggested to play a significant role in hand function; however, there are insufficient data to determine the strength of this association. This study aimed to investigate the correlation between hand function as measured with the Grooved pegboard test (GPT) and conduction velocity and latency of the median and ulnar nerves. We collected convenience samples in the College of Medicine, KSAU-HS. We used GPT to characterize hand function and performed measured nerve conduction velocity (NCV) and latency of the ulnar and median nerves of both hands. We used the Edinburgh handedness inventory (EHI) to determine hand dominance. We recruited 28 healthy medical students aged 20-29 years (mean: 21.46 ± 1.62 years). Most were right-handed (n = 25, 89.3%), with a mean EHI score of 302 ± 210. The mean GPT time was significantly faster in the dominant (65.5 ± 6.4 s) than in the non-dominant (75.0 ± 9.6 s) hand. The NCV for the ulnar nerve of the dominant hand was significantly correlated with GPT (r = -0.52, p = 0.005) while median nerve was not correlated (0.24, p = 0.21). Regression analysis and collinearity test showed that the ulnar NCV explained 20% of the variance in GPT of the dominant hand (R2 = 0.203, p = 0.016). The ulnar nerve conduction velocity, explained 20% of the variance in GPT times of the young men. Performance on this biomarker of neurological health seems to be more influenced by other factors in healthy young individuals.

Charcot–Marie–Tooth disease (CMT) is the most frequent form of inherited neuropathy with great variety of phenotypes, inheritance patterns, and causative genes. According to median motor nerve conduction velocity (MNCV), CMT is divided into demyelinating (CMT1) with MNCV below 38 m/s, axonal (CMT2) with MNCV above 38 m/s, and intermediate CMT with MNCV between 25 and 45 m/s. In each category, transmission may be autosomal dominant, autosomal recessive, or X-linked. The nosology of intermediate CMT is controversial because of concerns about electrophysiological delimitation. A systematic computer-based literature search was conducted on PubMed, using the following MeSH: (1) intermediate Charcot–Marie–Tooth; (2) X-linked intermediate Charcot–Marie–Tooth; and (3) X-linked Charcot–Marie–Tooth and electrophysiology. We retrieved 225 articles reporting X-linked CMT or intermediate CMT with electrophysiological information. After eligibility, 156 papers were used for this review. In assessing median MNCV, compound muscle action potential (CMAP) amplitudes were taken into account. In cases with attenuated CMAP and wherever possible, proximal median MNCV was used for accurate definition of conduction slowing in the intermediate range. In the vast majority of males with X-linked CMT associated with GJB1 mutation (CMTX1), median MNCV was intermediate. CMT associated with DRP2 mutation is another well-documented X-linked intermediate disorder. Autosomal dominant intermediate CMT (DI-CMT) encompasses 11 different types; six of them with assigned phenotype MIM number and the remaining five being unnumbered. Based on available electrophysiological information, we wonder if DI-CMTA should be reclassified within CMT2. Autosomal recessive intermediate CMT (RI-CMT) covers four numbered MIM phenotypes though, in accordance with reported electrophysiology, two of them (RI-CMTB and RI-CMTD) should probably be reclassified within AR-CMT2. We conclude that intermediate CMT is a complex inherited syndrome, whose characterization requires a specific electrophysiological protocol comprising evaluation of upper limb proximal nerve trunks when distal CMAP amplitudes are reduced, and that an updated version of MIM phenotype numbering is needed.

Leprosy neuropathy (LN) may cause demyelination that worsens during the leprosy reactions (LR). Type-1 LR (T1LR) occurs in patients with cell-mediated immune response against M. leprae, and Type-2 LR (T2LR) occurs in multibacillary cases. The patterns of nerve impairment need to be clarified, as both demyelination and axonal degeneration are commonly observed. This study aimed to describe how to interpret the demyelinating impairment in LN. Retrospective observational analysis of leprosy patients in a National Reference Center in Brazil between 2014-2023. 494 participants were included in this study. 3952 nerves were evaluated, with an average of 5.1 (±5.4) nerves affected per patient. 23.5% (116/494) of patients showed a demyelinating pattern defined by standard criteria, and 20.7% (24/116) presented exclusively demyelinating abnormalities without evidence of secondary axonal loss. 81% (94/116) presented conduction block, and 95.7% (111/116) temporal dispersion, with both conditions concomitant in 76.7% (89/116) of patients. 83.6% (97/116) demonstrated prolonged distal motor latency, and 99.1% (115/116) reduction in conduction velocity. 46.1% had T1LR and 17.9% T2LR. The comparison between patients with and without LR showed higher bacillary load, conduction block, and temporal dispersion in LR patients. 93.1% (108/116) of patients fulfilled neurophysiological criteria for chronic inflammatory demyelinating polyneuropathy (CIDP). Among them, 46.3% presented clinical criteria for atypical CIDP. Leprosy is a spectral disease in which neural damage can manifest in different phenotypes. Demyelinating impairment is frequent and varies according to the clinical form and presence of LR. Although demyelinating impairment is common in the studied population, it does not reflect active disease. LN can also be misdiagnosed as other peripheral neuropathies, especially CIDP, in non-endemic areas.